02 and respiratory failure

Question 1

what is type 1 respiratory failure?

Answer 1

• being short of oxygen with no impact of C02

Question 2

what is type 2 respiratory failure?

Answer 2

• short of oxygen

- too much C02

Question 3

what are the two mechanisms of type 1 respiratory failure?

Answer 3

• primary hypoxaemia in good lungs > increased Vt or increased RR (respiratory rate) > normal p02 and low pC02 > low p02 and normal pc02 = type 1
• primary hypoxaemia in bad lungs > low p02 and normal pC02

Question 4

what are the mechanism of type 2 respiratory failure?

Answer 4

• same as type 1 > low p02 and normal pC02 > low p03 and high pC02

Question 5

what produces acidosis?

Answer 5

• bad lungs > low p02 , high pC02 and normal HC03
  or
  low p02, very high pC02 and high HC03

Question 6

why can it be dangerous to give too much 02 to people?

Answer 6

it can lead to increased C02 and acidosis > uncontrollable lung damage

Question 7

what should be thought of when prescribing 02?

Answer 7

• oxygen is a drug
• only give is the risk/benefit ratio is in favour of it
• some people are very sensitive
• as p02 rises pC02 rises (acidosis, can be severe/ life threatening)

Question 8

which patients are at risk of type 2 respiratory failure?

Answer 8

• some COPD patients (1 in5)
• kyphoscoliosis
• end stage CF
• morbid obesity
  (nocturnal NIV - non invasive ventilation - is standard therapy for at risk groups )

Question 9

what happens in V/Q mismatching when excess 02 is given?

Answer 9

• areas of poor ventilation have reactive vasoconstriction
• give excess 02 and that reactive vasoconstriction reverses
• perfusion becomes good but ventilation is still poor

Question 10

Describe V and Q in a good lung.

Answer 10

in a normal lungs ventilation is good so localised oxygenation is good, there is vasodilation and goof perfusion V=Q

Question 11

Describe V and Q in a bad lung?

Answer 11

ventilation is poor so localised oxygen is poor, there is hypoxic vasoconstriction and poor perfusion. both V and Q are small.
- blood is redirected to areas of good ventilation and away from the poor areas

Question 12

what is the hypoxic drive theory?

Answer 12

• normal respiration is driven by C02 chemoreceptors
  -chronic hypercarbia (high C02) leads to desensitisation of these receptors
  -oxygen chemoreceptors then become the primary drive for respiration
  (effects small compared to Haldane effect and V/Q mismatching)

Question 13

what does V/Q mismatch tell us about the 02 that should be given?

Answer 13

patients with V/Q mismatch can be o2 sensitive

Question 14

how is hypercarbia treated?

Answer 14

• conservative 02 management

- increase Vminute (increased Vt with NIV)

Question 15

why is severe hypoxaemia bad?

Answer 15

• altered mental state, cyanosis, dyspnoea, tachypnoea, arrhythmias (tissue hypoxia)
• < 5.3 kPa = hyperventilation increases dramatically
• < 4.3 kPa = loss of consciousness
• <2.7 kPa = death

Question 16

what is the equation for tissue hypoxaemia?

Answer 16

DO2 (delivery of 02 to tissues) = CO X [(Hb x Sa02) + 0.003 x Pa02]

Question 17

Describe circulatory hypoxia

Answer 17

= hen oxygenated blood can’t get to the tissues

• global reduction = heart failure
• local reduction = obstruction of vessels, oedema, compression, compartments syndrome

Question 18

what is anaemic hypoxia?

Answer 18

B12 and folate deficiencies cause anaemia

• koilonychias (spooning of nails) is a characteristic sign of this
• not very common in western world
• blood loss can cause iron deficiency

Question 19

how does carbon monoxide poisoning occur?

Answer 19

• C0 binds irreversibly to Hb preventing 02 release and venous blood is therefore oxygenated
• cherry red venous blood is a sign and extremities can be bright red.

Question 20

what is hypoxaemic hypoxia?

Answer 20

= low inspired 02 conc.

e.g at high altitudes or as a result of the use of anaesthetics

Question 21

why might there be impaired diffusion?

Answer 21

• interstitial thickening (pulmonary fibrosis, lymphangitis, sarcoidosis)
• vascular dysfunction (pulmonary vasculitis, endothelial malignancy)

Question 22

what is:
A) perfusion without ventilations
B) ventilation without perfusion

Answer 22

A - shunting

B -dead space

Question 23

where is lung ventilation and perfusion good?

Answer 23

lung apex = good V poor Q

lung base = poor V good Q

Question 24

which patients should receive unrestricted 02 use?

Answer 24

• cluster headaches, carbon monoxide poisoning, pneumothorax which hasn’t been drained and sickle cell crisis

Question 25

Describe nasal cannulae.

Answer 25

• well tolerated
• low flow only
• uncontrolled Fi02
• dependant on nasal breathing

Question 26

Describe variable performance masks.

Answer 26

• cheap and simple
• 5-15 l/min
• uncontrolled Fi02
• unable to cope with high flow requirements

Question 27

Describe venture masks.

Answer 27

• fixed performance

- flows of up to 250 L/min

Question 28

Describe a non-rebreathing mask.

Answer 28

-Up to 85 % FiO2
-Uncontrolled FiO2
-Flow limited to outflow of wall
-Beware large VT
-Indications for this mask are now very few
(CO poisoningPTX
Cluster headaches
Sickling crisis)